John Libbey Eurotext. The Journal's web site is located at http://www.revue-stv.com

Citation

Sang Thrombose Vaisseaux, 1997, v. 9 n. 1, p. 22-30 How to Cite?

Abstract

Endothelial cell controls the tone of the underlying smooth muscle by releasing relaxing factors: nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF). G-proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin ADP-ribosylates selectively certain G-proteins (mainly Gi). In the porcine coronary artery, pertussis toxin inhibits the release of NO induced by certain (serotonin, α2-adrenergic agonists, leukotrienes, thrombin) but not all (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both Gi and Gp-proteins can couple receptor activation to the increase in endothelial Ca2+-concentration required to stimulate NO synthase. In arteries with regenerated endothelium, and in cultured endothelial cells, the release of NO by the pertussis toxin sensitive mechanism is reduced severely or is absent, while the response to other endothelium-dependent agonists is normal. To judge from experiments with cultured endothelial cells, the curtailment in pertussis toxin sensitive release of NO is due to abnormal function of rather than reduced presence of Gi proteins, or to reduced sensitivity of the cell membrane receptor. The selective impairment of Gi-proteins in regenerated endothelial cells predisposes the blood vessel wall to vasospasm and to the initiation of the atherosclerotic process.

Endothelial cell controls the tone of the underlying smooth muscle by releasing relaxing factors: nitric oxide (NO), prostacyclin and endothelium-derived hyperpolarizing factor (EDHF). G-proteins couple a number of endothelial cell receptors to the activation of NO synthase. Pertussis toxin ADP-ribosylates selectively certain G-proteins (mainly Gi). In the porcine coronary artery, pertussis toxin inhibits the release of NO induced by certain (serotonin, α2-adrenergic agonists, leukotrienes, thrombin) but not all (bradykinin, adenosine diphosphate) endothelium-dependent vasodilators. This suggests that both Gi and Gp-proteins can couple receptor activation to the increase in endothelial Ca2+-concentration required to stimulate NO synthase. In arteries with regenerated endothelium, and in cultured endothelial cells, the release of NO by the pertussis toxin sensitive mechanism is reduced severely or is absent, while the response to other endothelium-dependent agonists is normal. To judge from experiments with cultured endothelial cells, the curtailment in pertussis toxin sensitive release of NO is due to abnormal function of rather than reduced presence of Gi proteins, or to reduced sensitivity of the cell membrane receptor. The selective impairment of Gi-proteins in regenerated endothelial cells predisposes the blood vessel wall to vasospasm and to the initiation of the atherosclerotic process.

en_US

dc.language

eng

en_US

dc.publisher

John Libbey Eurotext. The Journal's web site is located at http://www.revue-stv.com